Neuroprotective Potential of Hericium Erinaceus aqueous extract utilization in ischemia-reperfusion injury related middle cerebral artery occlusion stroke model.

Abstract

Background: Globally, stroke is the elusive basis of sensory and motor impairments in humans. Multiple herbal compounds have been shown in studies to have positive therapeutic potential when used in conjunction with pharmaceutical therapies for the treatment and primary prevention of ischemic stroke. Current research investigation is planned to determine the neuro-protective potential of Hericium Erinaceus (HE) aqueous extract utilization in pre and post-middle cerebral artery occlusion (MCAO) model of ischemic–reperfusion injury. Methodology: Fifty-four Wistar albino rats (200-250 gms; 10-12 weeks) were divided into four experimental groups (n=9). Group I (control); Group II (sham); Group III (MCAO) MCAO for 20-30 min then 24 hours of reperfusion; Group IV was split into three groups as subgroup I (300 mg/kg BWT of AEHE given for 7 days), subgroup II (300 mg/kg BWT of AEHE given for 7 days and then MCAO), subgroup III (at the 4th hour of MCAO induction 300mg/kg of AEHE was given). Blood and cerebral, hepatic, and renal tissue samples were preserved and evaluated for modifications in plasma lipids levels, liver-kidney levels, c-reactive protein, blood glucose, and tissue antioxidant levels. A histopathological study was done over the selected tissues. Results: MCAO induction significantly alters the reno-hepatic profiles, c-RP levels, and animal tissue antioxidant (CAT, SOD, GSH) enzymes levels. However, HE-extract in both subgroups (Pre MCAO HE and Post MCAO HE) has significantly reduced lipid panel, glucose levels, and reno-hepatic parameters significantly. HE has effectively regulated antioxidant enzymes in cerebral, hepatic, and renal homogenates. In Pre-MCAO HE and Post-MCAO HE groups, the histopathological architecture of tissues is preserved. Conclusion: Daily dietary consumption of HE extract in calculated quantity significantly reduces the biochemical changes related to MCAO in a rat stroke model in ischemia-reperfusion injury.